| Stereochemistry | ACHIRAL |
| Molecular Formula | C12H10F2N2O3 |
| Molecular Weight | 268.2162 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
COC1=C(OC(F)F)C=CC(=C1)C2=NNC(=O)C=C2
InChI
InChIKey=HJMQDJPMQIHLPB-UHFFFAOYSA-N
InChI=1S/C12H10F2N2O3/c1-18-10-6-7(2-4-9(10)19-12(13)14)8-3-5-11(17)16-15-8/h2-6,12H,1H3,(H,16,17)
| Molecular Formula | C12H10F2N2O3 |
| Molecular Weight | 268.2162 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Zardaverine (6-(4-difluoromethoxy-3-methoxyphenyl)-3[2H]pyridazinone) is a dual-selective inhibitor of phosphodiesterase III/IV was developed as a potential therapeutic agent for asthma. Zardaverine has been shown to inhibit inflammatory cell function, human peripheral blood mononuclear cells (PBMC) and T-cell proliferation and exert a positive inotropic action on the heart muscle. In animals, zardaverine exhibits both bronchodilatory and anti-inflammatory activities. In order to study the efficacy and safety in man, Zardaverine has been tested in clinical trials for the treatment COPD and asthma. Zardaverine has a modest and short-lasting bronchodilatory effect in patients with asthma. However, due to its fast elimination, the development of zardaverine was terminated in 1991.
Originator
Approval Year
PubMed
Patents
Sample Use Guides
Zardaverine (at single doses of 1.5 mg, 3.0 mg, or 6.0 mg) was administered by metered dose inhaler
Route of Administration:
Respiratory
Zardaverine and anagrelide were tested in 16-point dose–response, comprising twofold dilutions from a top concentration of 7.5 μM, in a panel of malignant and non-malignant cell lines (CS242 embryonal rhabdomyosarcoma (ERMS), CS242 fibroblast, RD ERMS (ERMS of muscle origin), Rh18 ERMS, Rh36 ERMS, Normal female fibroblast, ERMS derived from paratesticular relapse, T24, HeLa). Compounds were tested in CS242 ERMS and RD ERMS seeded at 1,250 cells/well, and in CS242 fibroblast, normal female fibroblast, Rh18 ERMS, Rh36 ERMS, T24, and HeLa seeded at 313 cells/well. Cells were exposed to compound (0.1-10000nM) for 72 h at 37°C, 5% CO2. To determine cell viability, plates were allowed to cool to room temperature for 1 h after removal from 37°C incubation, 20 μl/well of CellTiter-Glo was added using a MicroFlo Select microplate reagent dispenser (BioTek, Winooski, VT, USA), and luminescence was measured after an additional 30 min at room temperature using an EnVision microplate reader (PerkinElmer, Waltham, MA, USA). Signal stability was confirmed by re-reading luminescence every 10 min for 2 h.
